tbuckley/cabot-search huggingface dataset:
Herbert Arthur Kent, M.R.C.S.Eng., L.R.C.P.Lond
Journal: BMJ (1904)

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Pre-B Cell Receptor-Mediated Activation of BCL6 Induces Pre-B Cell Quiescence Through Transcriptional Repression of MYC
Authors: Rahul Nahar, Parham Ramezani-Rad, Maximilian Mossner, Cihangir Duy, Leandro Cerchietti, Huimin Geng, Hassan Jumaa, B. Hilda Ye, Ari Melnick, Markus Muschen
Journal: Blood (2011)
Phase I study of the combination of alisertib (MLN8237) and gemcitabine in advanced solid tumors.
Authors: Edward Jae-hoon Kim, Thomas John Semrad, David R. Gandara, Jonathan Riess, Tianhong Li, Aiming Yu, Karen Matsukuma, Philip C. Mack, Karen Kelly
Journal: Journal of Clinical Oncology (2015)

2526 Background: Aurora Kinase A (AKA) is a key mitotic regulator overexpressed in multiple solid tumors. This open-label dose escalation phase I study evaluated the safety and tolerability of alisertib (MLN8237), an oral AKA inhibitor, in combination with gemcitabine. Methods: Patients (pts) > 18y with refractory solid tumors received 28-day cycles of gemcitabine on days 1, 8, 15 and alisertib twice daily on days 1-3, 8-10, and 15-17. Gemcitabine was given at a standard dose of 1000mg/m2. Four dose levels (DL) of alisertib (20-50mg) were planned following a conventional 3+3 design to investigate the occurrence of dose limiting toxicities (DLT) over cycle 1, and to determine the maximum tolerated dose (MTD) and recommended phase II dose (RP2D). Anti-tumor activity was assessed by response rate (RECIST 1.1) and progression-free survival. Results: Twenty-one pts were treated with median age 57 y [42-75]; 48% male; PS 0 (7 pts), 1 (13 pts), or 2 (1 pt); median prior therapies was 2 [0-7]; tumor types were NSCLC (7); colorectal (3); poorly differentiated neuroendocrine (3); small cell lung (2); head and neck (2); 1 each of pancreatic, gallbladder, small bowel, and mesothelioma. A median of 4 cycles [1-13] were administered. Two pts experienced DLTs: 1 pt at DL3 had grade 3 urinary tract infection; 1 pt at DL4 developed grade 3 oral mucositis, hyponatremia, and dehydration. The maximum administered dose (DL4) achieved 900 mg alisertib per cycle and was tolerated (1 DLT in 6 pts). Grade 3–4 hematologic toxicities observed included neutropenia (57%), leukopenia (48%), anemia (24%), and thrombocytopenia (14%). Hyponatremia (19%) was the only non-hematologic toxicity observed in > 10% of the pts. Ten of 14 evaluable pts (71%) had stable disease as their best response with remaining 4 pts having disease progression. Conclusions: Alisertib can be safely administered with gemcitabine and the R2PD for alisertib is 50 mg PO BID on days 1-3, 8-10, and 15-17 in combination with full dose gemcitabine. Further clinical evaluation of this combination is warranted and a pre-planned expansion is ongoing in pts with pancreatic adenocarcinoma including evaluation of pharmacokinetic interaction of the combination at the MTD. Clinical trial information: NCT01924260.
Outpatient Department Staff Members Pleased By Organization of Series of 'Specialty' Clinics
Journal: JAMA (1964)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Adrenoglomerulotropin
Authors: GORDON FARRELL
Journal: Circulation (1960)

The secretion of aldosterone by the zona glomerulosa of the adrenal cortex is controlled by a system which is not completely understood. Volume receptors are of importance although other receptors may be involved. The midbrain contains elements which influence the secretion of the steroid since lesions in this area of the brain stem reduce aldosterone output. A lipid factor, adrenoglomerulotropin, obtained from pineal extracts, selectively stimulates secretion of aldosterone; but a second factor, also from the pineal gland inhibits the output of aldosterone as well as of cortisol. It is suggested that the control of the secretion of aldosterone may be by an excitatory-inhibitory system involving the interplay of pituitary corticotropin, adrenoglomerulotropin and an anticorticotropin of pineal origin.
THE DEATH OF OLIVER WENDELL HOLMES.
Journal: JAMA (1994)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Maturational changes of endothelial vasoactive factors and pulmonary vascular tone at birth
Authors: M. Lévy, E. Souil, S Sabry, F Favatier, P Vaugelade, J.C Mercier, J Dall′ava-Santucci, A.T Dinh-Xuan
Journal: European Respiratory Journal (2000)

The aim of this study was to determine which endothelial factors were involved in the decrease of pulmonary vascular resistance at birth, and how they changed with maturation. Response of intrapulmonary artery rings precontracted with prostaglandin F2alpha were studied from piglets aged &lt;2 h, 2-3 day, 10 day and adult pigs for pharmacological responses to acetylcholine (ACh) and cromakalim (CMK) in the presence and the absence of the nitric oxide synthase (NOS) inhibitor, N(omega)-nitro-L-arginine (L-NA), the adenosine triphosphate sensitive potassium (K(ATP)) channel blocker, glibenclamide and the endothelin (ET)-A receptor antagonist, BQ123. In situ hybridization and immunochemistry studies were performed in lung tissues of the same animals in order to determine the expression of NOS and ET. There was a small contractile effect of ACh in the newborn. Relaxation to ACh, which was blocked by L-NA and reduced by glibenclamide, only appeared from the age of 3 days. The significantly greater relaxation to CMK in rings without endothelium (p&lt;0.05) was abolished by BQ123 in the newborn, and then disappeared by 2 days of age. Glibenclamide had a greater inhibitory effect on relaxation induced by CMK at 10 days than in the newborn and 2 days old piglets. NOS expression was low in pulmonary arteries of the newborn and increased by 2 days of age whereas the converse was seen with ET expression. It is concluded that: 1) relaxant response to acetylcholine was absent at birth and appeared at 2 days; 2) the reduced relaxant response to cromakalin in rings with endothelium at birth could be blocked by BQ123; and 3) the expression of endothelin decreased whereas the expression of nitric oxide synthase increased from birth to 2 days of age.
THE HARVEY SOCIETY.
Journal: JAMA (2005)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
American Journal of Mental Deficiency, Albany, NY
Journal: JAMA (1966)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
METABOLIC MISCONCEPTIONS
Journal: JAMA (1921)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Effects of Fiber Characteristics on Lung Deposition, Retention, and Disease
Authors: Morton Lippmann
Journal: Environmental Health Perspectives (1990)

There is abundant epidemiologic evidence that asbestos fibers can cause lung fibrosis (asbestosis), bronchial cancer, and mesothelioma in humans, as well as limited evidence for such effects in workers exposed to slag and rockwool fibers. Epidemiological evidence for human disease from inhalation exposures to conventional fibrous glass is negative. While health concerns based on the morphological and toxicological similarities between man-made fibers and asbestos are warranted, it is important to note that most of the toxicological evidence for glass fiber toxicity in laboratory animals is based on nonphysiological exposures such as intratracheal instillation or intraperitoneal injection of fiber suspensions. Man-made fibers have produced lung fibrosis and mesotheliomas in such tests, albeit at much lower yields than asbestos. For all durable mineral fibers, critical length limits must be exceeded to warrant concern about chronic toxicity; i.e., 2 microns for asbestosis, 5 microns for mesothelioma, and 10 microns for lung cancer. Fiber width must be less than 0.1 microns for mesothelioma, and larger than this limit for asbestosis and lung cancer. The human health risks for most fibrous glass products are either low or negligible for a variety of reasons. First, most commercial fibrous glass products have mean fiber diameters of approximately 7.5 microns, which results in mean aero-dynamic diameters approximately 22 microns. Thus, most glass fibers, even if dispersed into the air, do not penetrate into the lung to any great extent. Second, the small fraction of smaller diameter fibers that do penetrate into the lungs are not persistent within the lungs for most fibrous glass products due to mechanical breakage into shorter lengths and overall dissolution.(ABSTRACT TRUNCATED AT 250 WORDS)
Modulation of intracellular calcium by depolarization and G-coupled agonists in isolated cultured rat liver endothelial cells 2, Andr�-Viallet Clinical Research Center1, H�pital St-Luc and Membrane Transport Research Group2, U. de Montr�al, Montr�al, Qu�bec
Journal: Hepatology (1995)

The generation of NO by endothelial nitric oxide synthase (eNOS) plays a major role in maintaining cardiovascular homeostasis. The objective of our present study was to investigate the effects of the flavone compound, apigenin, on eNOS activity and elucidate the molecular mechanisms underlying these effects in endothelial cells (ECs).Bovine artery endothelial cells (BAECs) were exposed in a serum-free medium to apigenin. Cell viability was measured using an Alamar blue assay. The production of intracellular NO was determined using DAF-2/DA. The level of protein was examined by Western blotting. The intracellular Ca2+ was measured using a fluorescent dye, Fura 2-AM.Apigenin significantly induced NO production after 6 h of treatment. This production was inhibited by pretreatment with the eNOS inhibitor, Nω-nitro l-arginine methyl ester (L-NAME). However, treatment with apigenin did not alter the eNOS protein levels but induced a sustained activation of eNOS Ser1179 phosphorylation. Apigenin was further found to activate ERK1/2, JNK and Akt over various time courses in ECs. Treatment with specific PI3-kinase inhibitors significantly inhibited the increases in NO production and phosphorylation. In contrast, the inhibition of (ERK)1/2, JNK and p38 had no influence on NO production. In addition, apigenin stimulates an increase in the cytosolic Ca2+ concentration. Apigenin-induced eNOS Ser1179 phosphorylation and NO production are calcium-dependent, as pretreatment with extracellular or intracellular Ca2+ chelators inhibits these processes.Apigenin-induced calcium-dependent activation of eNOS is primarily mediated via phosphatidylinositol 3-kinase- and Akt pathways, and occurs independently of the eNOS protein content.
Effect of Various Treatments on Toxicity of Inhaled Vinylidene Chloride
Authors: Robert D. Short, Joseph M. Winston, Jan L. Minor, Joseph Seifter, Cheng-Chun Lee
Journal: Environmental Health Perspectives (1977)

The toxicity of vinylidene chloride (VDC) was studied in mice and rats exposed to various concentrations of the vapors for 23 hr/day. In addition, the ability of various treatments to alter parameters of toxicity was evaluated. Mice were more sensitive than rats both to the acute lethal and hepatotoxic effects of VDC. Disulfiram treatment reduced the acute lethal and hepatotoxic effects of inhaled VDC and reduced the levels of covalent bound radioactivity in the liver and kidney after the intraperitoneal administration of 14C-VDC. Treatment with diethyldithiocarbamate and thiram also protected mice from the acute lethal effects of VDC.
Highlights
Journal: JAMA (2015)

In a randomized, open-label study that enrolled 399 patients who were hospitalized with an acute pulmonary embolism (PE) and had a high risk of recurrent PE, Mismetti and colleagues assessed the effi cacy and safety of retrievable vena cava fi lter placement plus anticoagulation therapy vs anticoagulation therapy alone for prevention of recurrent PE.The authors report that use of a retrievable inferior vena cava fi lter plus anticoagulation, compared with anticoagulation alone, did not reduce the risk of symptomatic recurrent PE at 3 months' follow-up. ED-Initiated Buprenorphine for Opioid Dependence 1636Emergency department (ED) screening, brief intervention, and referral for treatment has shown effi cacy for some forms of unhealthy substance use.In a randomized, single-center trial that enrolled 329 opioid-dependent patients, D'Onofrio and colleagues assessed the effi cacy of 3 ED interventions for opioid dependence: screening and referral to treatment; screening, a Brief Negotiation Interview intervention, and facilitated referral to community-based treatment services; or screening with brief intervention, treatment initiation with buprenorphine, primary care follow-up, and addiction treatment referral.The authors found that individuals randomly assigned to receive ED-initiated buprenorphine with primary care follow-up were signifi cantly more likely to engage in formal addiction treatment than were participants receiving the alternative interventions in the ED.
Abemaciclib Shows Promise for Early Breast Cancer
Journal: Cancer Discovery (2016)

Treatment with the CDK4/6 inhibitor abemaciclib, alone or in combination with endocrine therapy, significantly lowered expression of the protein Ki67-a key marker of cell proliferation-in women with hormone receptor-positive, HER2-negative breast cancer. The findings from the phase II neoMONARCH trial suggest that CDK4/6 inhibition may be effective for neoadjuvant treatment of early breast cancer.
Dementia
Authors: Esther S. Oh, Peter V. Rabins
Journal: Annals of Internal Medicine (2020)

Letters4 February 2020DementiaEsther S. Oh, MD, PhD and Peter V. Rabins, MD, MPHEsther S. Oh, MD, PhDJohns Hopkins University School of Medicine, Baltimore, Maryland (E.S.O., P.V.R.) and Peter V. Rabins, MD, MPHJohns Hopkins University School of Medicine, Baltimore, Maryland (E.S.O., P.V.R.)Author, Article, and Disclosure Informationhttps://doi.org/10.7326/L19-0682 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:We appreciate Dr. Finucane's comment about the French government's decision to delist the acetylcholinesterase inhibitors donepezil, galantamine, and rivastigmine. In our article, we state, "When the benefit is unclear, use of acetylcholinesterase inhibitors or memantine may be stopped." We also note, "Patients and families may need help in developing realistic expectations for these agents." Furthermore, we list some of the more common adverse effects associated with these medications.Our recommendations are in line with those from the American Geriatrics Society, which state, "Clinicians, patients, and their caregivers should discuss treatment goals of practical value that can be easily ...References1. American Geriatrics Society. Ten things clinicians and patients should question. Updated 23 April 2015. Accessed at www.choosingwisely.org/societies/american-geriatrics-society on 20 December 2019. Google Scholar2. AGS Choosing Wisely Workgroup. American Geriatrics Society identifies another five things that healthcare providers and patients should question. J Am Geriatr Soc. 2014;62:950-60. [PMID: 24575770] doi:10.1111/jgs.12770 CrossrefMedlineGoogle Scholar Author, Article, and Disclosure InformationAffiliations: Johns Hopkins University School of Medicine, Baltimore, Maryland (E.S.O., P.V.R.)Disclosures: Disclosures can be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=M19-1237. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoDementia Esther S. Oh and Peter V. Rabins Dementia Thomas E. Finucane Metrics 4 February 2020Volume 172, Issue 3Page: 226KeywordsCaregiversCholinesterase inhibitorsCognitionDementiaDisclosureGeriatricsMotivation ePublished: 4 February 2020 Issue Published: 4 February 2020 Copyright & PermissionsCopyright © 2020 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Hepatocellular carcinomas associated with hepatitis B and C virus infections: Are they any different?
Authors: K OKUDA
Journal: Hepatology (1995)

It is known among liver specialists that hepatocellular carcinoma (HCC) among southern African blacks is quite different clinically as well as histopathologically from that in other ethnic g r o u p ~. l -~ As early as 1960, Steiner4 performed a pathological study on cirrhosis and HCC in sub-Saharan Africa, and observed more frequent poorly differentiated HCC associated with less severe cirrhosis and inflammation in blacks compared with HCC among whites in Los Angeles and Chicago.Berman's monograph on primary liver cancer published in 19515 described in detail the clinically relentless progression of the disease among Mozambican blacks.Subsequent studies have shown that hepatitis B surface antigen (HBsAg) carrier rates do not vary much among Bantu blacks,6 but there is a ninefold difference in HCC incidence between the Mozambicans living along the coast and in the inland.7It is generally believed based on such studies that exposure to aflatoxin is the major etiological factor in certain areas in Africa and elsewhere,8 and that the degree of exposure to aflatoxin makes differences in incidence and biology of the cancer.It seemed that more investigators were interested in elucidating differences between chemically and virally induced HCC, and not too many attempts were made to determine whether hepatitis B virus (HBV)-associated HCC has any characteristic features compared with etiologically differing HCC.In this issue of HEPATOLOGY, Shiratori et a19 report their clinical observations of 205 cases of HCC seen at the University of Tokyo Hospital in 1990 to 1993 that consisted of 173 patients with hepatitis C virus (HCV) antibodies (Ab), 25 patients with HBsAg (2 overlapping cases), and 9 patients negative for both.They analyzed various clinical and epidemiological parameters.The average age was younger in HBsAg-positive cases.Only one half of them had cirrhosis, and the remaining half had moderately active chronic hepatitis.By contrast, patients with HCV-Ab-positive HCC more fre-~~